Birthweight, childhood growth and left ventricular structure at age 60-64 years in a British birth cohort study

BACKGROUND: High left ventricular mass (LVM) is an independent predictor of cardiovascular disease and mortality, but information relating LVM in older age to growth in early life is limited. We assessed the relationship of birthweight, height and body mass index (BMI) and overweight across childhood and adolescence with later life left ventricular (LV) structure. METHODS: We used data from the MRC National Survey of Health and Development (NSHD) on men and women born in 1946 in Britain and followed up ever since. We use regression models to relate prospective measures of birthweight and height and BMI from ages 2–20 years to LV structure at 60–64 years. RESULTS: Positive associations of birthweight with LVM and LV end diastolic volume (LVEDV) at 60–64 years were largely explained by adult height. Higher BMI, greater changes in BMI and greater accumulation of overweight across childhood and adolescence were associated with higher LVM and LVEDV and odds of concentric hypertrophy. Those who were overweight at two ages in early life had a mean LVM 11.5 g (95% confidence interval: -2.19,24.87) greater, and a mean LVEDV 10.0 ml (3.7,16.2) greater, than those who were not overweight. Associations were at least partially mediated through adult body mass index. Body size was less consistently associated with relative wall thickness (RWT), with the strongest association being observed with pubertal BMI change [0.007 (0.001,0.013) per standard deviation change in BMI 7–15 years]. The relationships between taller childhood height and LVM and LVEDV were explained by adult height. CONCLUSIONS: Given the increasing levels of overweight in contemporary cohorts of children, these findings further emphasize the need for effective interventions to prevent childhood overweight

Concordance of sibling's recall of measures of childhood socioeconomic position

<p>Abstract</p> <p>Background</p> <p>Studies of socioeconomic determinants of health often rely on recalled information on childhood socioeconomic position, despite limited evidence of the validity of this information. This study examined concordance between siblings of recalled measures of childhood socioeconomic position.</p> <p>Methods</p> <p>This cross-sectional study examined reports by 1280 adult sibling pairs in the National Survey of Midlife Development in the United States of seven measures of childhood socioeconomic position: father's occupation (in 9 categories), father having a professional occupation, father being a supervisor at work, father's education level, mother's education level, receipt of welfare payments, and subjective appraisal of being better or worse off financially than others.</p> <p>Results</p> <p>Concordance was high for father's professional occupation (0.97; 95% confidence interval (CI) 0.96, 0.98), father's occupation in 9 categories (0.76; 95% CI 0.73, 0.80), and receipt of welfare payments (0.95; 95% CI 0.93, 0.97). Concordance was lower for father's and mother's education level, and lowest for subjective appraisal of socioeconomic position (0.60; 95% CI 0.57, 0.64). Concordance of parental education was lower for sibling pairs with high school educations or less.</p> <p>Conclusion</p> <p>Concordance of recalled measures of childhood socioeconomic position by siblings is generally but not uniformly high.</p

The emergence of health inequalities in early adulthood: evidence on timing and mechanisms from a West of Scotland cohort

Background Evidence is inconsistent as to whether or not there are health inequalities in adolescence according to socio-economic position (SEP) and whether or when they emerge in early adulthood. Despite the large health inequalities literature, few studies have simultaneously compared the relative importance of ?health selection? versus ?social causation? at this life-stage. This study followed a cohort through the youth-adult transition to: (1) determine whether, and if so, when, health inequalities became evident according to both class of origin and current SEP; (2) compare the importance of health selection and social causation mechanisms; and (3) investigate whether these phenomena vary by gender. Methods Data are from a West-of-Scotland cohort, surveyed five times between age 15 (in 1987, N=1,515, response=85%) and 36. Self-reported physical and mental health were obtained at each survey. SEP was based on parental occupational class at 15, a combination of own education or occupational status at 18 and own occupational class (with an additional non-employment category) at older ages. In respect of when inequalities emerged, we used the relative index of inequality to examine associations between both parental and own current SEP and health at each age. In respect of mechanisms, path models, including SEP and health at each age, investigated both inter and intra-generational paths from SEP to health (?causation?) and from health to SEP (?selection?). Analyses were conducted separately for physical and mental health, and stratified by gender. Results Associations between both physical and mental health and parental SEP were non-significant at every age. Inequalities according to own SEP emerged for physical health at 24 and for mental health at 30. There was no evidence of selection based on physical health, but some evidence of associations between mental health in early adulthood and later SEP (intra-generational selection). Paths indicated intra-generational (males) and inter-generational (females) social causation of physical health inequalities, and intra-generational (males and females) and inter-generational (females) social causation of mental health inequalities. Conclusions The results suggest complex and reciprocal relationships between SEP and health and highlight adolescence and early adulthood as a sensitive period for this process, impacting on future life-chances and health

Systemic Inflammation and Cardio-Renal Organ Damage Biomarkers in Middle Age Agre Associated with Physical Capability Up to 9 Years Later: Findings from a British Birth Cohort Study

BACKGROUND: Physical capability, a key component of healthy aging, is associated with cardiovascular and other risk factors across life. We investigated whether midlife biomarkers of heart and kidney damage capturing the cumulative impact of long-term adverse exposures were associated with the level and decline in physical capability over 9 years of follow-up, taking account of systemic inflammatory biomarkers and conventional cardiovascular risk factors. METHODS: We used data on 1736 men and women from the oldest British birth cohort study with walking speed, chair rise speed, balance time, and grip strength assessed at ages 60 to 64 and 69 years. We tested associations between logged and standardized measures of cystatin C, NT-proBNP (N-terminal pro-Btype natriuretic peptide), interleukin (IL)-6, and E-selectin at age 60 to 64 years with performance at age 69 years, adjusting for sex, height, and body mass index; then for performance at age 60 to 64 years. These biomarkers were mutually adjusted, and additionally adjusted for cardiovascular risk factors (pulse pressure, total/high density lipoprotein cholesterol, glycosylated hemoglobin), diabetes mellitus, cardiovascular and kidney disease, smoking status, and lifetime socioeconomic position. RESULTS: Cystatin C, NT-proBNP, and IL-6 (but not E-selectin) were inversely associated with all outcomes, adjusted for sex, height, and body mass index. For example, a 1-SD increase in logged NT-proBNP was associated with weaker grip (−0.63 kg, 95% CI, −0.99 to −0.28); the equivalent association for cystatin C was −0.60 kg (95% CI, −0.94 to −0.25) and for IL-6 was −0.76 kg (95% CI, −1.11 to −0.41). Most associations remained, albeit attenuated, after adjustment for previous performance and mutual adjustment of the biomarkers. NT-proBNP and IL-6 (but not cystatin C) were more strongly associated with the outcomes than many of the conventional risk factors after mutual adjustment. CONCLUSIONS: Higher levels of NT-proBNP may identify those in midlife at risk of accelerated physical decline. Before considering the use of NT-proBNP for risk stratification, further research should untangle whether these associations exist because the biomarker is an integrated measure of cumulative exposures to relevant stressors across life, or whether it is marking additional risk pathways. Randomized trials to reduce the rate of decline in physical capability or delay incident disability could benefit from including middle-aged adults and adding NT-proBNP and IL-6 as intermediate outcomes